Neuroprotective Efficiency of Cyclosporine After Traumatic Brain Injury in Rats

The level of brain edema was evaluated through the wet-dryweight method, the lipid peroxidation ratio, and histological examination by transmission electron microscopy.RESULTS: The level of brain edema and lipid peroxidation ratio significantly decreased in the rats that received cyclosporine.Ultrastructural neurodestruction was graded, and a comparison of the scores between the experimental groups revealed significantneuroprotective effects of cyclosporine.CONCLUSION: The results demonstrated that systemic administration of cyclosporine produces a statistically significant decreasein both the level of brain edema and lipid peroxidation ratio when compared with “no treatment”.

📌 3 Key Takeaways

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Objective & Hypothesis:AIM: To evaluate the possible neuroprotective effects of systemic administration of cyclosporine (Cyclosporin A) after traumaticbrain injury in rats.MATERIAL and METHODS: The modified Feeney method was used as the trauma model in male Sprague Dawley rats.

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Key Findings & Data:After thetrauma, 20 mg/kg of cyclosporine was administered to the one group of the rats (n=12) intraperitoneally.

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Conclusion & Impact:The level of brain edema was evaluated through the wet-dryweight method, the lipid peroxidation ratio, and histological examination by transmission electron microscopy.RESULTS: The level of brain edema and lipid peroxidation ratio significantly decreased in the rats that received cyclosporine.Ultrastructural neurodestruction was graded, and a comparison of the scores between the experimental groups revealed significantneuroprotective effects of cyclosporine.CONCLUSION: The results demonstrated that systemic administration of cyclosporine produces a statistically significant decreasein both the level of brain edema and lipid peroxidation ratio when compared with “no treatment”.

🔬Design:Modeling & Simulation

📍Scope:Comprehensive Sample

⚙️Variables:Domain Parameters

Özet

AIM: To evaluate the possible neuroprotective effects of systemic administration of cyclosporine (Cyclosporin A) after traumaticbrain injury in rats.MATERIAL and METHODS: The modified Feeney method was used as the trauma model in male Sprague Dawley rats. After thetrauma, 20 mg/kg of cyclosporine was administered to the one group of the rats (n=12) intraperitoneally. Twenty-four hours afterinjury, the subjects were sacrificed, and brain samples were removed. The level of brain edema was evaluated through the wet-dryweight method, the lipid peroxidation ratio, and histological examination by transmission electron microscopy.RESULTS: The level of brain edema and lipid peroxidation ratio significantly decreased in the rats that received cyclosporine.Ultrastructural neurodestruction was graded, and a comparison of the scores between the experimental groups revealed significantneuroprotective effects of cyclosporine.CONCLUSION: The results demonstrated that systemic administration of cyclosporine produces a statistically significant decreasein both the level of brain edema and lipid peroxidation ratio when compared with “no treatment”. Cyclosporine, which is regularlyused as an immunosuppressant agent, is also known to prevent opening of the mitochondrial permeability transition pore byunbinding mitochondrial matrix cyclophilin. Regulation of transition pore for mitochondrial permeability by cyclosporine implies thatmitochondrial dysfunction following traumatic brain injury is an important event in the progressive loss of neuronal tissue.

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Cite This Article

GÜRCAN, O., UÇKUN, Ö. M., CELIKMEZ, R. C., TÜRKOĞLU, Ö. F., EROGLU, H., BEŞKONAKLI, E., ÖNER, L., TASKIN, Y. (2020). Neuroprotective Efficiency of Cyclosporine After Traumatic Brain Injury in Rats. Turkish Neurosurgery, Cilt: 30 - Sayı: 4, 507–512. https://ajindex.com/articles/404309

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References (1)

Ankarcrona M, Dypbukt JM, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton SA, Nicotera P: Glutamate induced neuronal death: A succession of necrosis or apoptosis depending on mitochondrial function. Neuron 15:961-973,1995 2. Borlongan CV, Yu G, Matsukawa N, Xu L, Hess DC, Sanberg PR, Wang Y: Acute functional effects of cyclosporine-A and methylprednisolone treatment in adult rats exposed to transient ischemic stroke. Life Sciences 76: 1503-1512, 2005 3. Diaz-Ruiz A, Rios C, Duarte I, Correa D, Guizar-Sahagun G, Grijalva I, Ibarra A: Cyclosporin-A inhibits lipid peroxidation after spinal cordinjury in rats. Neurosci Lett 266:61-64,1999 4. Domanska-Janika K, Buzanska L, Dluzniewska J, Kozlowska H, Sarnowska A, Zablocka B: Neuroprotection by cyclosporin A following transient brain ischemia correlates with the inhibition of the early efflux of cytochrome C to cytoplasm. Mol Brain Res 121:50-59, 2004 5. Engelborghs K, Verlooy J, Van Reempts J, Van Deuren B, Van De Ven M, Borgers M: Temporal changes in intracranial pressure in a modified experimental model of closed head injury. J Neurosurg 89:796-806, 1998 6. Eroglu H, Kas H, Oner L, Turkoglu OF, Akalan N, Sargon MF, Ozer N: The in-vitro and in-vivo characterization of PLGA: L-PLA microspheres containing dexamethasone sodium phosphate. J Microencapsul 18:603-612, 2001 7. Feeney DM, Boyeson MG, Linn RT, Murray HM, Dail WG: Responses to cortical injury: i. Methodology and local effects of contusions in the rat. Brain Res 211:67-67, 1981 8. Graham DI, Mcintosh TK, Maxwell WL, Nicoll JAR: Recent advances in neurotrauma. J Neuropathol and Exp Neurology 59: 641-651, 2000 9. Guha A: Management of traumatic brain injury: Some current evidence and applications. Postgrad Med J 80:650-653, 2004 10. Laurer HL, Lenzlinger PM, McIntosh TK: Models of traumatic brain injury. Eur J Trauma 26:95-100, 2000 11. Maxwell RE, Long DM, French LA: The effects of glucosteroids on experimental cold-induced brain edema gross morphological alterations and vascular permeability changes. J Neurosurg 34:477-487, 1971 12. Murakami K, Kondo T, Yang G, Chen SF, Morita-Fujimura Y, Chan PH: Cold injury in mice: A model to study mechanisms of brain edema and neuronal apoptosis. Prog Neurobiol 57:289-299, 1999 13. Okonkwo DO, Melon DE, Pellicane AJ, Mutlu LK, Rubin DG, Stone JR, Helm GA: Dose response of cyclosporin a in attenuating traumatic axonal injury in rat. Neuropharm and Neurotox 14:463-466, 2003 14. Okonkwo DO, Povlishock JT: An intrathecal